These studies have two general goals, both related to the use of glucocorticoids in treatment of leukemias and lymphomas. One goal is to apply and extend our knowledge of glucocorticoid receptors and mechanisms of action to normal and malignant lymphocytes and related cells (including cells from patients) in order to understand how various glucocorticoid-receptor complexes are related to direct glucocorticoid effects on the cells. For these studies we will apply our recently developed methods for rapidly separating cytoplasmic glucocorticoid-receptor complexes into "nonactivated," "activated" and mero-receptor forms, to complexes from the various cells mentioned, under various conditions. One of our first goals is to use these methods to compare the stability of complexes from various cells. With cells from patients, we will attempt to use our results to refine correlations between receptors and response to therapy. The other goal is to extend our observations on indirect glucocorticoid effects on lymphocytes and other cells that are mediated by inhibition of lymphokines such as T-cell growth factor (TCGF) and Fc-Receptor Augmenting Factor (FRAF). FRAF, as we have recently demonstrated, is probably identical to gamma interferon. In the case of TCGF, we will study production of this factor by malignant lymphoid cells, sensitivity of the cells to TCGF, and the influence of glucocorticoids on production. In the case of FRAF, we will begin to study glucocorticoid mechanisms of inhibition of its production, and some of the physiological and therapeutic implications of this inhibition.